ReviewExperimental & molecular medicine2025
The multifaceted role of YAP in the tumor microenvironment and its therapeutic implications in cancer.
Review in Experimental & molecular medicine, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
26 citing papers in PubMed.
- Single-cell epigenomics of colorectal cancer.Experimental & molecular medicine · 2026Review
- Hippo Pathway-YAP/TAZ Signaling: Molecular Mechanisms, Biological Function, Diseases, and Therapeutic Targets.MedComm · 2026Review
- Platycodon grandiflorus-Derived Nanovesicles Sensitize Gastric Cancer to T Cell Killing via Ferroptosis-Driven Membrane Mechanical Remodeling.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- Early SOX9 Activation Primes Hippo-YAP/TAZ Rewiring During Glioblastoma Stemness Acquisition.Journal of cellular and molecular medicine · 2026Article
- Recent Advances in Genetically Engineered Mouse Models of Melanoma: Insights into Tumor Initiation and Oncogenic Signaling Pathways.International journal of stem cells · 2026Review
- The Crosstalk Between YAP/TAZ and Cancer Metabolism: From Mechanistic Insights to Drug Discovery.International journal of molecular sciences · 2026Review
- CD47 and FOXP3Cancers · 2026Review
- Review
- Mechanobiology-Driven Metabolic Reprogramming: Integrative Roles of YAP/TAZ Signaling and Extracellular Matrix Dynamics.Cell biology international · 2026Review
- Cancer-associated fibroblasts as a target in head and neck squamous cell carcinoma: bridging mechanisms to therapy with drugs, adjuvants, and nanotechnology.Discover oncology · 2026Review
- The mechano-immunological landscape in the tumor microenvironment: From mechanical sensing to a new therapeutic paradigm.Materials today. Bio · 2026Review
- Mitochondrial Metabolic Reprogramming in Colorectal Cancer-Associated Fibroblasts: An Up-to-Date Review.Cancers · 2026Review
- Conserved principles of central carbon partitioning in Hippo-Yorkie-drivenbioRxiv : the preprint server for biology · 2026Article
- Article
- Research on the Hippo Pathway in Cancer.Cells · 2026Review
- Mechanobiology of the Hippo-YAP Signaling Network.Cold Spring Harbor perspectives in biology · 2026Article
- Mechanobiology of cancer-associated thrombosis: from molecular mechanisms to therapeutic innovation.Journal of nanobiotechnology · 2026Review
- Targeting phase separation: a new strategy to disrupt the stromal-immune axis in colorectal cancer.Cell communication and signaling : CCS · 2026Review
- The APC/C subunit APC7 promotes hepatocellular carcinoma progression by mediating ubiquitination and degradation of LATS1 to activate YAP/TAZ.Biology direct · 2026Article
- Tumor suppressor network dysregulation in neuroblastoma: molecular mechanisms and precision therapeutic opportunities.Frontiers in cell and developmental biology · 2026Review
Corrections and comments
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Authors and funding
2 authors.
Funding
Abstract
The tumor microenvironment (TME) plays a critical role in cancer progression, immune evasion and therapeutic resistance. The transcriptional coactivators YAP and TAZ, key effectors of the Hippo signaling pathway, have emerged as central regulators of TME remodeling. YAP/TAZ are activated in both tumor and stromal compartments, where they function as mechanotransducers and integrate canonical Hippo pathway suppression, noncanonical microenvironmental cues and genetic or epigenetic signals to drive transcriptional programs. These changes collectively facilitate tumor immune evasion. YAP/TAZ further promote angiogenesis and upregulate PD-L1 expression in tumor cells and cancer-associated fibroblasts, and a subset of immunosuppressive cells in the TME, contributing to resistance to ICB. In addition to their tumor-intrinsic and stromal functions, YAP/TAZ impair antitumor immunity by altering immune cell differentiation and dampening effector responses. Targeting the YAP/TAZ-TEAD axis has shown potential efficacy when combined with immune checkpoint inhibitors, chimeric antigen receptor T cell therapies and tumor vaccines. Although challenges such as tumor selectivity and resistance mechanisms persist, advances in single-cell and spatial transcriptomics are enabling the dissection of YAP/TAZ-regulated networks and guiding the development of more precise therapeutic strategies. Collectively, YAP/TAZ inhibition offers a promising avenue to reprogram the TME and enhance the efficacy of next-generation cancer immunotherapies.
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Registered trials
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